Dietary β-conglycinin prevents acute ethanol-induced fatty liver in mice

• Mice fed β-conglycinin prevented acute ethanol-induced fatty liver.
• β-Conglycinin suppressed ethanol-induced activation of PPARγ2 and its target genes.
• β-Conglycinin downregulated basal expression of genes related to de novo lipogenesis.

Alcoholic fatty liver is the earliest stage of alcohol-induced liver disease leading to liver cirrhosis. β-Conglycinin, one of the soy proteins, is known to prevent non-alcoholic fatty liver, hyperlipidemia and obesity. Therefore, we examined whether β-conglycinin feeding has an effect on the prevention of acute ethanol-induced fatty liver in mice. Male C57BL/6J mice were fed with 20 energy% β-conglycinin or casein for 4 weeks prior to ethanol administration and were then given ethanol or glucose, as a control, by gavage. Ethanol significantly increased liver triglyceride (TG) in mice fed casein due to the activation of peroxisome proliferator-activated receptor (PPAR) γ2, a nuclear transcription factor known for regulating lipid metabolism and de novo lipogenesis. The liver TG of ethanol-administered β-conglycinin-fed mice was significantly lower than that in those fed casein, although ethanol increased the amount of liver TG in mice fed β-conglycinin. The increased levels of PPARγ2 protein and its target gene CD36 in response to an ethanol were not observed in mice fed β-conglycinin. Moreover, β-conglycinin decreased the basal expression of de novo lipogenesis-related genes such as stearoyl-CoA desaturase-1, and therefore, the expressions of these genes were lower in the ethanol-administered β-conglycinin-fed mice than in the casein-fed mice. In conclusion, β-conglycinin supplementation appears to prevent the development of fatty liver in mice caused by ethanol consumption via the suppression of alcohol-induced activation of PPARγ2 and the downregulation of the basal expression of de novo lipogenesis.

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